Wednesday, October 12, 2011

Initial assessment of seriously ill patient

Hello again,thank you for visiting my blog, forgive me for not writing the topics nicely or the way it should be. I prefer those topic to be discussed in such manner.I am busy and still nothing is done in order. I am worried, nothing is done according to timeline and I am very desperate to reach my goals for this year.


I have started a new interest since I am the coordinator of the advance skill center in my department. I observed that the gap in between knowledge and practical is so real. Previously, the students are given a scenario that is not in the orderly way and results in chaotic debriefing sessions. I am glad to share one of the scenario here. I teach very basic stuff, that include patient safety. My students enjoyed the simulation class but I understand that it is not easy to immerse in the scenario and treat the manikin as a 'real patient'. I noticed, the students lack of adrenaline and always 'asking for some gadgets to drop down from the sky'.


SIMULATION BASED LEARNING: WORKSHOP FOR YEAR 4, SPECIALIZED POSTINGThere are two components of the workshop.
1. Introduction to human patient simulator
2. Airway workshop

1. Introduction to human patient simulator-bridging the gap between theory and practice.
General objectives: Week 1
1. Understand the principles of assessment of seriously ill patient
2. Introduction to patient safety
a. I.V. cannulation
b. Preparation of intravenous drip
c. Breaking ampoules and dilution of drugs
d. Patient monitor
3. Handling of defibrillator machine
Venue: ECS room, Advance Clinical Skill Centre, Kulliyyah of Medicine, IMC
Equipments: METI Emergency care simulator, fully equipped emergency room, emergency trolley, I.V. cannulation tray, IV drip and solution, drugs, syringes, defibrillation machine, NIBP, devices for oxygen therapy,
Normal 12 leads ECG, ABG, CXR with pneumonic changes/pneumothorax
Week 2: Assessment of patient in emergency situation:
Scenario 1:25 year old male patient is presenting with a sudden onset of shortness of breath. He has a history of asthma and occasionally uses an inhaler. This asthma attack had a sudden onset. He is very anxious and unable to speak in complete sentences. He appears exhausted.
Allergies: Penicillin
Medications: Occasional albuterol inhaler
Social History: Smoker
Secondary assessment: 70kg, 5’8”, sitting up with obvious difficulty breathing, appears to be leaning over in an effort to catch his breath. He is sweating and in obvious distress.
Objectives:
1. Able to apply the principle of assessment of unstable patient
• Targeted history
• Focused physical examination
• Order Investigations
• Identify abnormal physiology
• Treatment of abnormal physiology
• Differential diagnosis and ‘Best guess’ diagnosis
2. CVS and Respiratory examination
• Recognize abnormal breath sounds
3. Immediate Management of acute exacerbation of bronchial asthma
• Salbutamol nebulizer
• IV hydrocortisone
• Consider antibiotics
4. Recognize easy ABG abnormalities
5. Application of monitors and ECG
6. IV cannulation and IV fluid therapy
7. Initial investigations
N.B. Patient is not allowed to die. The scenario is terminated after all objectives are achieved or they have reached a point whereby it is too dangerous to continue.

Notes for the lecturers:

ASSESSMENT OF UNSTABLE PATIENT
• It is recommended to use a systemic approach to assessment to ensure that all immediately life threatening problems are recognized and the correct treatment is started immediately.
• Critically ill patients often have multiple problems and the use of systemic approach reduces the risk of missed diagnoses and provides a framework for treatment when working under stressful conditions.
• You are interested in all patients’ problems and their responses to the treatments instigated.
The aim of assessment of seriously ill patient is to:1• Identify the life-threatening pathophysiological abnormalities
2• Identify the most appropriate way to correct those abnormalities
3• Diagnose the underlying problem
In emergency, tasks that are typically carried out sequentially often have to be carried out in parallel with history taking (targeted history), examination (focused examination) and initial resuscitation often occurring simultaneously. Treatment is initiated on a “best guess” basis rarely enough time to be certain of cause prior to starting resuscitation. Important to realize that response to treatment needs to be made every few minutes not every few hours. The working diagnosis needs to be repeatedly reassessed as more information becomes available and on the basis of response to treatment.
The focus of subsequent examination is to determine the underlying cause, in order to determine the appropriate definitive therapy.
The first step in assessing a seriously ill patient is to estimate how ill the patient is and how much time is available for assessment and investigation before initiating treatment.
• Assessing the compensatory response to the primary abnormality. This involves activation of the sympathetic nervous system and magnitude of such response. In the pre-terminal patient, this compensatory response id exhausted
• The intensity of supportive therapy e.g. the degree of oxygen therapy and oxygen saturation.

Immediate assessment
A Airway (patency) assessment and treatment if needed
B Breathing assessment and treatment if needed
C Circulation assessment and treatment if needed
D Dysfunction of the central nervous system
E Exposure sufficient to allow complete examination

Process of ABC assessment in an acutely ill patient is predominantly clinical and follows the simple clinical pattern of Look, listen and feel.
In dire emergencies (true emergencies) , e.g. airway obstruction, tension pneumothorax, ventricular dysrhythmias, pericardial tamponade, exsanguination and hypoglycaemia you have to own the airway, breathing (thorax) and circulation (heart, blood vessels).

A-AIRWAYTalk to patient, a patient who is able to respond appropriately must at that moment have control of their airway and have adequate oxygenation, ventilation and cerebral circulation to be able to reply coherently.
• LOOK – for the presence of
cyanosis,
obstructed pattern of respiration or abdominal breathing,
Use of accessory muscles of respiration
Tracheal tug
Alteration in level of consciousness
Any obvious obstruction by foreign body or vomit
• LISTEN
For abnormal sounds such as grunting, snoring, gurgling, hoarseness or stridor
• FEEL
For airflow on inspiration and expiration
If an obstruction is present then the immediate goal must be to obtain and secure the airway to allow oxygenation and ventilation. As soon as airway is patent, high concentration of oxygen should be administered.
-Chin lift or jaw thrust
-Suction to remove secretions
-Oral airway is inserted in obtunded patients.
-Patients can be oxygenated by using bag and mask ventilation.
If simple method fails, definitive airway is indicated. If patient is at extremis, intubation may be accomplished without the use of drugs. If patient is responsive, intubation is done with anaesthetic drugs. Attempts at intubation without first preoxygenating the patient are futile and dangerous
If above steps unsuccessful, surgical airway should be performed with cricothyroidotomy being the method of choice.
B- BREATHINGA respiratory rate of less than 12 or more than 30 breath/min, inability to speak in complete sentences because of breathlessness or breathlessness at rest, are all sinister signs of impending respiratory failure. Marked tachypnea is a useful marker of a severely ill patient, regardless of whether the patient has respiratory failure.
• LOOK for:
Central cyanosis
Use of accessory muscles of respiration
High or low respiratory rate
Equality and depth of respiration,
Sweating
Raised JVP
Patency of chest drains
Presence of any paradoxical abdominal or chest wall movement.
Abdominal distension
Note the inspired oxygenation and saturation if pulse oximetry is in use, but remember that pulse oximetry does not detect hypercarbia.
• LISTEN for:
Noisy breathing, audible wheeze, clearance of secretions by coughing
Ability of patient to talk in complete sentences (evidence of confusion or decreased level of consciousness may indicate hypoxia or hypercarbia, respectively)
Change in percussion note
Auscultate for abnormal breath sounds, heart sounds and rhythm
• FEEL for
Equality of chest movement,
Position of trachea
Presence of surgical emphysema or crepitus
Paradoxical respiration
Tactile vocal fremitus if indicated
The best treatment will be determined by the cause and severity of the respiratory failure.

You should look for the signs of immediately life-threatening conditions of tension pneumothorax, massive hemothorax, flail chest and cardiac tamponade and provide immediate appropriate treatment.
Remember that the chest drains may become dislodged or blocked and that their presence does not exclude recurrent pneumothorax. Simple maneuvers such as sitting the patient up can help, but if the patient is tiring to the point of respiratory arrest then assisted ventilation by bagging may be necessary until help arrives.


C-CIRCULATIONAll shocked surgical patients should be assumed to be hypovolemic until proved otherwise
• LOOK for
Reduce peripheral perfusion (pallor, coolness, collapsed or under-filled veins) – remember blood pressure may be normal in the shocked patient. As a result of compensatory mechanisms hypotension is a late feature of cardiovascular dysfunction.
Obvious external haemorrhage from either wound or drains
Evidence of concealed haemorrhage into the abdomen, pelvis, soft tissues or thorax. An empty drain does not exclude the presence of concealed bleeding.
• LISTEN to
Heart sounds: gallop, rhythm, quiet heart sounds or a new murmur may indicate a primary cardiac problem.
• FEEL for
Peripheral and central pulses, assessing volume equality and rhythm.
Unless there are obvious signs of cardiogenic shock (e.g. raised JVP and gallop rythm ) venous access with a 16G cannula should be obtained, blood sent for cross-matching and other routine tests, including clotting screen, and appropriate fluid replacement started: rapid fluid challenge of 10ml/kg or 20ml/kg if patient is hypotensive. Patient with heart failure should receive an initial bolus of 5 ml/kg and closer monitoring may be needed.
If patient is actively bleeding from a non-compressible source, then the correct treatment is surgical control. Fluid resuscitation should be maintained at levels to maintain organ perfusion while surgery is being arranged.



D-DYSFUNCTION OF THE CNSA rapid assessment may obtained by using mnemonic AVPU
A-Alert and orientated
V-vocalizing
P-responding only to pain
U-unconscious

• If time permits, a full Glasgow Coma Scale should be performed as this is a more repeatable and objective measurement of consciousness.
• Alteration of conscious level may be due to intracranial and extracranial causes. Hypoxia, hypercarbia, cerebral hypoperfusion, sedatives or opioid drugs may be responsible. Metabolic or endocrine causes should be considered, notably hypoglycaemia (DEFG=don’t ever forget glucose), uraemia or hypothyroidism. If the diagnosis is not obvious, review the ABCs.
• A marked reduction in conscious level indicates either that compensatory homeostatic mechanisms have been overwhelmed or severe neurological disease. Urgent supportive therapy is advocated. The pupillary response should be checked frequently.


E-EXPOSURE• The patient must be exposed to allow full examination, and the environment should be warm to prevent hypothermia.
• There should be adequate light, and preserving the patient’s privacy by the use of screens is essential. If intimate examinations are planned then a chaperone is required.


At the end of initial assessment the patient should hopefully have a secure airway, with adequate oxygenation, ventilation and circulation.
Commence monitoring of vital signs, including pulse, blood pressure, temperature, urine output and pulse oximetry. At this stage consider the need for specialist help and advice, the requirement for additional investigations and the level of care the patient needs. Do not leave the patient until he/she is stable.
Initial investigations:
ABGs, glucose, ECG, electrolytes, full blood count, CXR
In subsequent assessment, other investigations should be ordered on the basis of the history and clinical findings.
Summary
Beware of patients who demonstrate any of the following features, especially if they are acute in onset or severe. Patients with a greater number of these features are likely to be sicker.
1. Altered level of conscious state
2. Hypotension
3. Tachycardia
4. Tachypnea
5. Cyanosis/hypoxia
6. Oliguria
7. Acidosis


Debriefing:
Debriefing is done at two levels, during the scenario (pause and discuss technique) and at the end of scenario (with or without videotaping). The lecturers must understand the goals of debriefing, the importance of it, various techniques and process of debriefing.
The process of debriefing:
1. Introduction
2. Personal reaction
3. Discussion of events
4. Summary

Sunday, July 24, 2011

antifungal agents

Antifungals: Triazole, Polyene and echinocandin
1. Triazole
-inhibits ergosterol synthesis in the fungal cell wall by inhibiting lanosterol demethylase
-examples: fluconazole, itraconazole, voraconazole
-all azoles can cause hepatotoxicity, anaemia, thrombocytopenia, leukopenia, stevens-johnson syndrome, multiple drug interactions - increase levels of phenytoin, warfarin, cyclosporin

2. Polyene
-combines with sterols in fungal membrane to create a channel with leakage of cytosol
-e.g. Amphotericin, nystatin

3. Echinocandin
-inhibit synthesis of D-glucan, a key fungal cell wall component
-e.g. caspofungin, micafungin

Saturday, July 23, 2011

what is right is always seen as wrong

Hi again,
thank you guys for visiting my site, it is not great but at least there are some important facts are discussed here.
The world that we live in is a mystery. It is very disheartening when people maybe talk and support about certain values, but on the other hand are fighting against the same facts and ideas.
I am trying to educate people at my work place based on my knowledge, expertise and experience, but people are uncomfortable and prefer to live in ignorance. Recently, I was asked to lower my expectation and quality of practice to their extremely dangerous level instead of striving to improve themselves. The irony is they wanted to be treated like adults but on the other hand required to be told all the instructions step-by-step.
My reminder to them is, alright...you can live in that situation but I won't because I want to live with the Physician's Oath that I had taken upon graduation 21 years ago. I keep wondering why they make it customary for us to read that oath out aloud if it is something that is not going to be lived by.

Monday, April 4, 2011

High frequency ventilation

Currently HFOV is used as salvage therapy for patients failing conventional mechanical ventilation. It should restricted to centres with training and experience in this mode of ventilation. HFOV provides tidal volume below the anatomic dead space at frequencies greater than 60 breaths per second.

Benefits include reduce barotrauma, improve V/Q matching and less respiratory compromise. Complications include dessication and inspissation of mucus, airway damage due to high gas velocities, air trapping and high shear forces at interfaces between areas of the lung at different impedences.



Gas exxchange during HFOV:



  • direct bulk flow


  • longitudinal (taylor) dispersion


  • pendeluft


  • asymmetric velocity profile


  • cardiogenic mixing


  • molecular diffusion


1. Two observational studies, adults who failed to respond to conventional ventilation were managed with HFOV at 5 Hz. Improvement in oxygenation were noted within 8 hours in both studies. (Fort CCM 1997, Mehta CCM 2001).


2. HFOV for ARDS in adults: a RCT. Derdak AJRCCM 2002.

Multicentre Oscillatory Ventilation for ARDS Trial (MOAT)

148 adults were randomised to HFOV or conventional ventilation. The HFOV group had significant improvement in oxygenation within 16 hours,compared to conventional ventilation. However the improvement did not persist and oxygenation was the same in both groups by 24 hours. The survival trend favour HFOV over CV but is underpowered (would need n=199 to evaluate mortality)


The difference in survival rate did not reach significance at 30 or 90 days.



3. High frequency oscillatory ventilation in adults: the Toronto experience. Mehta Chest 2004 Canadian experience, Retrospective chart review of 156 patients treated with HFOV. The authors suggested that HFOV might be an effective rescue therapy for patients with severe oxygenation failure. Because mortality was associated with a greater number of days receiving conventional ventilation prior to HFOV, the authors also suggested that earlier institution of HFOV could be beneficial.



4. High Frequency Oscillatory Ventilation Compared to Conventional Ventilation in ARDS: a RCT. Bollen et al. Crit Care 2005

ICU in London, Cardiff, Paris, Mainz. n = 61

Study stopped prematurely because of la ow inclusion rate and the completion of similar MOAT trial.

No difference in 30 day mortality. Post hoc analysis- better treatment effect of HFOV in patients with higer baseline oxygen index (OI).


Critics: Small number of patients, lack of explicit ventilation protocol and underpowered to show differences in efficacy or safety.


Conclusions:


1. HFOV as safe and efficacious as lung protective controlled ventilation in RCTs.

2. There is a trend of improved mortality with HFOV but this needs to be repeated in a fully powered, properly controlled RCT.

3. HVOV may be more effective in patients with high baseline OI, but this should be studied directly.




Thrombocytopenia in critically ill patients


 

 

 

 

Definition:

  1. Plt count less than 150, 000/micL, generally not significant until less than 100,000.
  2. Relative  thrombocytopenia - acute drop from a higher platelet count may be pathologic.

Pathophysiology:


1. Decreased production
 a) Isolated thrombocytopenia
 b) Multiple cytopenias
2. Increased destruction and consumption

 a) Immune or alloimmune: primary (idiopathic) or secondary -associated with other autoimmune disease (e.g. SLE), associated with malignancy, maybe complication of infection and drug associated thrombocytopenia

b) Nonimmune -isolated or combined platelet consumption
3. Increased sequestration in enlarge spleen

a) portal hypertension
b) myloproliferative disease
c) lymphoma
d) storage and infiltrative deseases of spleen
e) chronic hemolysis
f) granulomatoses -eg tuberculosis, sarcoidosis

4. Dilutional - effect of massive transfusion and fluid resuscitation

5. States with multiple causes of thrombocytopenia:

a) cirrhosis with portal hypertension
b) hepatitis
c) HIV
d) other viral illnesses
e) patients with multiple medical problems on multiple drugs


Diagnosis


  1. FBP with peripheral smear: -Review of rbc abnormalities e.g. schistocytes, teardrops, nucleated RBC. Rule out pseudothrombocytopenia due to platelet clumping.
  2. Coagulation testing: Identify associated coagulation abnormalities
  3. Additional blood tests, if required:  
  • viral titres and antibodies
  • autoimmune disorders (e.g. collagen vascular disease)
  • other disorders

     4. Radiologic
  • abdominal US -evaluation of spleen size
  • CT scan -evaluation for lymphoproliferative disease

    5. Indication for bone marrow examination

  • unclear pathology
  • multiple cytopenias
  • suspected infiltrative process

Therapy


1. Transfusion therapy indications:

  • bleeding or necessary invasive procedures
  • prophylactic - for very severe (less than 10,000) thrombocytopenia
  • other blood components as indicated to correct coagulation abnormalities

2. Platelet transfusion relatively contraindicated:
  • TTP unless bleeding present
  • ITP unless bleeding present
  • HIT without bleeding - unknown

3. Primary thrombocytopenia - depends on specific disorder

4. Secondary thrombocytopenia -direct therapy at underlying causes

Saturday, April 2, 2011

Propofol Infusion Syndrome

Propofol is an intravenous anesthetic that is commonly used for sedation in ICU. the elimination of propofol is not impaired by hepatic or renal dysfunction. Propofol has a large volume of distribution and is highly protein bound. During administration serum triglycerides should be monitored in all patients who receive propofol in doses > 50 mcg/kg/min for more than 2 days. If hypertriglyceride is detected, alternative should be considered. Unusual and potentially serious complications are associated with continous infusion of propofol for longer tnan 24 to 48 hours. These include progressive hyperglyceridaemia, pancreatitis, increased carbon dioxide production and excessive caloric load (the emulsion contains approcimately 1.1 kcal/ml, most of which derived from lipids).
Propofol Infusion Syndrome (PRIS): PRIS is a rare complication of propofol for longer than 24 to 48 hours. It is associated with high doses ( more than 4 mg/kg/hour of mone than 67 mcg/kg/min) and prolonged use (more than 48 hr). Characteristic of the syndrome include acute refractory bradycardia, severe metabolic acidosis, CVS collapse, rhabdomyolysis, hyperlipidaemia, renal failure and hepatomegaly. Mortality is high, more than 60% in a study. Risk factors:

  • large doses and duration more than 48hrs

  • younger age

  • acute neurological injury

  • low carbohydrate intake

  • catecholamine and corticosteroid infusion

Clinical and lab findings:


  • unexplained lactic acidosis

  • increasing inotropic support

  • Brugada like ECG abnormalities

  • Green urine

  • CVS collapse

  • rhabdomyolysis, high CK, hyperkalaemia

  • arrythmia/ heart block

  • renal failure

Management:


  1. high index of suspicion

  2. discontinue infusion immediately

  3. monitor for early warning signs: lactate, CK, urine myoglobin, ECG

  4. standard cardiorespiratory support

  5. consider pacing for bradycardia ( often resistant to high dose of CA )

  6. adequate carbohydrate intake

  7. ECMO: 2 case reports

  8. haemoperfusion and haemodialysis are used with uproven benefit

  9. carnitine supplementation: theoretical benefit

Sunday, March 27, 2011

Extracorporeal membrane oxygenation (ECMO)

1. Extracorporeal membrane oxygenation for 2009 Influenza (H1N1) ARDS - ANZ ECMO influenza investigators. Journal: JAMA, Oct 19, 2009 A descriptive analysis of all adult and paediatric (neonates excluded) patients treated with ECMO, 1st june - 31 August 2009 in Australia, NZ ICU's during 2009 H1N1 epidemic. In 200 ICUs, 15 supplied ECMO for 61 (32%) of 194 H1N1/ Influenza A ventilated patients with 21% mortality. All these patients met inclusion criteria for the CESAR trial. to be continued..

Saturday, March 26, 2011

MRI pearls


  1. FLAIR - fluid attenuated inversion recovery sequence eliminates the signal from CSF. it is sensitive to oedema and inflammation. Axial T2 FLAIR: nulls the normally bright T2 signal of CSF (becomes black), while other parenchymal fluid appears bright (as in oedema or tumour).

  2. Diffusion Weighted Imaging (DWI) DWI assesses the movement of protons due to diffusion over a short time. If there is restricted diffusion the signal is of high intensity. If there is unrestricted diffusion (e.g. CSF), there is low intensity signal. Unfortunately the signal on DWI is not just produced by the diffusion characteristics but also changes in parallel with the T2 and PD of the tissue. To eliminate these cofounders an apparent diffusion coefficient (ADC) map is generated. The ADC signal is low with true restricted diffusion. Using a combination of these sequences vasogenic oedema (intensity high on T2, high on DWI and high on ADC map) may be distinguished from cytotoxic oedema (intensity high on T2, high on DWI and reduced on ADC map).

  3. Gadolinium contrast: Gd is a paramagnetic substance that acts as a contrast agent by markedly shortening T1 when it is present. Gd based contrast distributes throughout the extracellular fluid, and does not cross the normal BBB. In pathological conditions in which the BBB breaks down, there is marked hyper-intensity (enhancement) of affected areas on T1 weithted images.